• Angela Starkweather, Linda Witek-Janusek, and Herbert L Mathews.
• Washington State University, Intercollegiate College of Nursing, 2917 West Fort George Wright Drive, Room 369, Spokane, WA 99224, USA. astarkweather@wsu.edu
• Biol Res Nurs. 2005 Jan 1;6(3):196-206.

AbstractBidirectional communication between the immune system and the brain and the implications of this communication are emerging concepts in pain research. Although representing a small portion of the disc degeneration syndromes, lumbar herniated discs can cause significant symptoms that may persist even after surgical interventions. Evolving evidence demonstrates that proinflammatory cytokines are a key mediator in the process of disc degeneration as well as in the pain experienced by those afflicted with lumbar herniated discs. Activated immune cells release proinflammatory cytokines, which signal the brain through humoral and neural routes. The brain responds by altering neural activity and promoting further production of proinflammatory cytokines within the brain and spinal cord. Increased local cytokine production by disc tissue irritates spinal nerve roots, resulting in pain and functional changes in neural activity. This review of the current literature explores the importance of cytokine production within the context of lumbar disc degeneration and lumbar spine pain. Furthermore, the significance of the neural-immune interaction will be examined as it relates to pain management and to patient treatment.

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